To understand better the pathogenesis of filarial infections (onchocerciasis, loiaisis, lymphatic filarasis) clinical assessments of patients with these and other related non-filarial (strongyloides, malaria) infections have been studied in detail. Moreover, the post-treatment inflammatory responses and the underlying mechanisms in their induction have been detailed. In particular, the control of eosinophil induction and cell trafficking to sites of post-treatment inflammation has been studied. The importance of the Wolbachia endosymbiont both as a therapeutic target and as a inducer of inflammation has been detailed as well.[unreadable] [unreadable] The pathogenesis of lymphedema in lymphatic filariasis has been shown to result (in part) from interdigital lesions that predispose to acute lymphangioadenitis.[unreadable] [unreadable] Understanding of the pathogenesis of eosinophil-related disorders has been a major focus of our clinically related studies. Multiple groups of hypereosinophilic patients (parasite-infected, familial hypereosinophilia, idiopathic hypereosinophilic syndrome, benign hypereosinophilia, episodic angioedema with eosinophilia) have been assessed clinically; moreover, lymphocytes (and their subsets) and eosinophils have been examined functionally and at the molecular level (human microarrays and RT-PCR) to identify the molecules and pathways involved in conditions associated with increased blood and tissue eosinophilia.